Lactaturia and loss of sodium-dependent lactate uptake in the colon of SLC5A8-deficient mice.
Level 5 - mechanism / opinion, no new human data
Animal knockout study (mechanistic and preclinical research).
PubMed 18562324 · doi:10.1074/jbc.M802681200
What was done
Researchers generated SLC5A8-deficient mutant mice (Slc5a8-/-) to determine the in vivo physiological functions of the transporter. They examined lactate handling in the kidney proximal tubules, serous salivary gland ducts, and colonocytes, evaluated thyroidal apical iodide transport in wild-type and SLC26A4-deficient backgrounds, and tested the proposed tumor suppressor role by exposing mice to carcinogens and breeding them onto the Apc(min) background.
What was found
SLC5A8 was found to mediate apical lactate re-absorption in proximal tubules and salivary ducts, as well as sodium-dependent lactate uptake into colonocytes, with deficiency leading to lactaturia. SLC5A8 was not essential for thyroid apical iodide transport. Furthermore, Slc5a8-/- mice did not display an increased incidence of tumor formation following carcinogen exposure or when crossed with Apc(min) mice. The abstract provides qualitative directional findings and contains no numerical data.
Why it matters
This study establishes that SLC5A8 functions primarily as a monocarboxylate transporter involved in renal and colonic lactate conservation rather than a critical thyroid iodide transporter or tumor suppressor in mice.
Limits
Findings are derived entirely from mouse models and may not fully translate to human physiology. The abstract reports no quantitative values, sample sizes, or effect sizes, and evaluation was limited to specific carcinogen and Apc(min) tumor models.
Cited by
- supports The intestinal lactate transporter belongs to a different gene family than the monocarboxylate transporters in cell membranes and functions as a sodium symport rather than a proton symport.